Avoidant/Restrictive Food Intake Disorder: a Three-Dimensional Model of Neurobiology with Implications for Etiology and Treatment

Purpose of Review DSM-5 defined avoidant/restrictive food intake disorder (ARFID) as a failure to meet nutritional needs leading to low weight, nutritional deficiency, dependence on supplemental feedings, and/or psychosocial impairment. We summarize what is known about ARFID and introduce a three-di...

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Bibliographic Details
Published in:Current psychiatry reports 2017-08, Vol.19 (8), p.54-54, Article 54
Main Authors: Thomas, Jennifer J., Lawson, Elizabeth A., Micali, Nadia, Misra, Madhusmita, Deckersbach, Thilo, Eddy, Kamryn T.
Format: Article
Language:English
Subjects:
Eating Disorders (S Wonderlich and JM Lavender
Etiology
Feeding and Eating Disorders - classification
Feeding and Eating Disorders - etiology
Feeding and Eating Disorders - physiopathology
Feeding and Eating Disorders - therapy
Humans
Medicine
Medicine & Public Health
Neurosciences
Psychiatry
Section Editors
Topical Collection on Eating Disorders
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Summary:Purpose of Review DSM-5 defined avoidant/restrictive food intake disorder (ARFID) as a failure to meet nutritional needs leading to low weight, nutritional deficiency, dependence on supplemental feedings, and/or psychosocial impairment. We summarize what is known about ARFID and introduce a three-dimensional model to inform research. Recent Findings Because ARFID prevalence, risk factors, and maintaining mechanisms are not known, prevailing treatment approaches are based on clinical experience rather than data. Furthermore, most ARFID research has focused on children, rather than adolescents or adults. We hypothesize a three-dimensional model wherein neurobiological abnormalities in sensory perception, homeostatic appetite, and negative valence systems underlie the three primary ARFID presentations of sensory sensitivity, lack of interest in eating, and fear of aversive consequences, respectively. Summary Now that ARFID has been defined, studies investigating risk factors, prevalence, and pathophysiology are needed. Our model suggests testable hypotheses about etiology and highlights cognitive-behavioral therapy as one possible treatment.
ISSN:1523-3812
1535-1645
DOI:10.1007/s11920-017-0795-5